ReviewMedical sciences (Basel, Switzerland)2017
Cytokine Signaling in Multiple Sclerosis and Its Therapeutic Applications.
Review in Medical sciences (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.
- Elucidating the bidirectional association between autoimmune diseases and depression: a systematic review and meta-analysis.BMJ mental health · 2024Pooled it
- IL-6 and TNF-α responses to acute and regular exercise in adult individuals with multiple sclerosis (MS): a systematic review and meta-analysis.European journal of medical research · 2022Pooled it
- 1,3,4 oxadiazole derivative attenuates neurotransmitter-mediated inflammatory response in EAE model of multiple sclerosis.Scientific reports · 2026Article
- Fluorine-18-labeled PET radiotracers for imaging the macrophage colony-stimulating factor 1 receptor (CSF1R).EJNMMI radiopharmacy and chemistry · 2026Article
- Cytokine Gene Expression and Treatment Impact on MRI Outcomes in Jordanian Patients with Multiple Sclerosis.Life (Basel, Switzerland) · 2025Article
- Profiling Blood-Based Neural Biomarkers and Cytokines in Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis Using Single-Molecule Array Technology.International journal of molecular sciences · 2025Article
- New serum soluble factors predicting inflammatory and non-inflammatory disability worsening in multiple sclerosis.Frontiers in immunology · 2025Article
- Loss of Cullin 5 in myeloid cells protects against autoimmune neuroinflammation.Frontiers in immunology · 2025Article
- COVID-19 vaccines and neurological disorders: A narrative review of immune responses and adverse reactions.AIMS neuroscience · 2025Review
- Can Vitamin D Supplementation Improve Inflammation in Relapsing-Remitting Multiple Sclerosis Patients?Biomedicines · 2024Article
- Can Vitamin D Reduce Inflammation? The Influence of Supplementation on Selected Immunological Markers.International journal of molecular sciences · 2024Article
- Article
- Cytokines, Vascular Endothelial Growth Factors, and PlGF in Autoimmunity: Insights From Rheumatoid Arthritis to Multiple Sclerosis.Immune network · 2024Review
- The brain cytokine orchestra in multiple sclerosis: from neuroinflammation to synaptopathology.Molecular brain · 2024Review
- The fluctuations of expression profiles of critical genes in the miRNA maturation process and pro-and anti-inflammatory cytokines in the pathogenesis and progression of multiple sclerosis.Molecular biology reports · 2023Article
- Imaging of Tauopathies with PET Ligands: State of the Art and Future Outlook.Diagnostics (Basel, Switzerland) · 2023Review
- Integration of epigenetic and genetic profiles identifies multiple sclerosis disease-critical cell types and genes.Communications biology · 2023Article
- NLRP3 inflammasome in neurodegenerative disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Arginine vasopressin hormone receptor antagonists in experimental autoimmune encephalomyelitis rodent models: A new approach for human multiple sclerosis treatment.Frontiers in neuroscience · 2023Review
- CD40 Drives Central Nervous System Autoimmune Disease by Inducing Complementary Effector Programs via B Cells and Dendritic Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is one of the most common neurological disorders in young adults. The etiology of MS is not known but it is widely accepted that it is autoimmune in nature. Disease onset is believed to be initiated by the activation of CD4+ T cells that target autoantigens of the central nervous system (CNS) and their infiltration into the CNS, followed by the expansion of local and infiltrated peripheral effector myeloid cells that create an inflammatory milieu within the CNS, which ultimately lead to tissue damage and demyelination. Clinical studies have shown that progression of MS correlates with the abnormal expression of certain cytokines. The use of experimental autoimmune encephalomyelitis (EAE) model further delineates the role of these cytokines in neuroinflammation and the therapeutic potential of manipulating their biological activity in vivo. In this review, we will first present an overview on cytokines that may contribute to the pathogenesis of MS or EAE, and provide successful examples and roadblock of translating data obtained from EAE to MS. We will then focus in depth on recent findings that demonstrate the pathological role of granulocyte-macrophage colony-stimulating factor (GM-CSF) in MS and EAE, and briefly discuss the potential of targeting effector myeloid cells as a treatment strategy for MS.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.